Santicioli P, Del Bianco E, Tramontana M, Maggi C A
Pharmacology Department, A. Menarini Pharmaceuticals, Florence, Italy.
Neurosci Lett. 1992 Sep 14;144(1-2):211-4. doi: 10.1016/0304-3940(92)90752-s.
Electrical field stimulation (5 Hz) evoked a prompt outflow of calcitonin gene-related peptide- and substance P-like immunoreactivities (CGRP-LI and SP-LI, respectively) from superfused slices of the dorsal but not ventral half of the rat spinal cord. The evoked outflow was abolished by tetrodotoxin, calcium-free medium or previous exposure to capsaicin, indicating that it is produced through action potentials invading the central terminals of capsaicin-sensitive primary afferents. Adenosine as well as gamma-aminobutyric acid (GABA) or the GABAB receptor agonist (-)-baclofen produced a concentration-dependent inhibition of the evoked CGRP-LI outflow. Adenosine also inhibited the evoked SP-LI outflow. These findings demonstrate that inhibition of transmitter release from primary afferent neurons should be considered as a possible mechanism of the antinociceptive action of adenosine and adenosine analogs.
电场刺激（5赫兹）可促使降钙素基因相关肽样免疫反应物质和P物质样免疫反应物质（分别为CGRP-LI和SP-LI）从大鼠脊髓背侧而非腹侧半部分的灌流切片中迅速流出。河豚毒素、无钙培养基或先前接触辣椒素可消除这种诱发的流出，表明它是通过动作电位侵入辣椒素敏感的初级传入神经的中枢终末产生的。腺苷以及γ-氨基丁酸（GABA）或GABAB受体激动剂（-）-巴氯芬对诱发的CGRP-LI流出产生浓度依赖性抑制。腺苷也抑制诱发的SP-LI流出。这些发现表明，抑制初级传入神经元的递质释放应被视为腺苷和腺苷类似物抗伤害感受作用的一种可能机制。
